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Biomedical subjects

P Tchou

Publications and source records attributed to P Tchou.

At least 19 recordsLinked to original sources
PubMed2001

Ventricular tachycardias arising from the aortic sinus of valsalva: an under-recognized variant of left outflow tract ventricular tachycardia.

OBJECTIVES: To describe a normal heart left bundle branch block, inferior axis ventricular tachycardia (VT), that could not be ablated from the right or left ventricular outflow tracts. BACKGROUND: Whether these VTs are epicardial and can be identified by a specific electrocardiographic pattern is unclear. METHODS: Twelve patients with normal heart left bundle branch block, inferior axis VT and previously failed ablation were included in this study. Together with mapping in the right and left ventricular outflow tracts, we obtained percutaneous epicardial mapping in the first five patients and performed aortic sinus of Valsalva mapping in all patients. RESULTS: No adequate pace mapping was observed in the right and left ventricular outflow tracts. Earliest ventricular activation was noted in the epicardium and the aortic cusps. All patients were successfully ablated from the aortic sinuses of Valsalva (95% CI 0% to 18%). The electrocardiographic pattern associated with this VT was left bundle branch block, inferior axis and early precordial transition with Rs or R in V2 or V3. Ventricular tachycardia from the left sinus had rS pattern in lead I, and VT from the noncoronary sinus had a notched R wave in lead I. None of the patients had complications and all remained arrhythmia-free at a mean follow-up of 8 +/- 2.6 months. CONCLUSIONS: Normal heart VT with left bundle branch block, inferior axis and early precordial transition can be ablated in the majority of patients from either the left or the noncoronary aortic sinus of Valsalva.

Adolescent↗
PubMed2001

Empirical pulmonary vein isolation in patients with chronic atrial fibrillation using a three-dimensional nonfluoroscopic mapping system: long-term follow-up.

The purpose of this study was to assess the feasibility and long-term results of empirical isolation of both superior pulmonary veins in patients with chronic AF. Although localizing and ablating the focal triggers of AF has been proven an effective approach, this strategy is time consuming, often requires multiple procedures, and carries the risk of pulmonary vein stenosis. Whether ostial electrical isolation of the superior pulmonary veins, without initial detailed mapping, is a more efficient approach is not known. The study included 71 consecutive patients who had chronic AF. Using a nonfluoroscopic electroanatomic mapping system, the left and right superior pulmonary veins were ablated circumferentially at the venoatrial junction, with the aim of achieving electrical isolation of the veins. Following ablation, if frequent atrial ectopies were present, mapping and ablation were considered. The patients were periodically followed with 48-hour Holter and loop recorder monitoring. After the ablation of the right and left superior pulmonary veins 59 (83%) of 71 patients maintained sinus rhythm without premature atrial beats. The remaining 12 patients underwent further mapping and ablation including 5 patients who required isolation of the left inferior pulmonary veins. True electrical isolation could be achieved only in 45 (31%) of the 147 targeted veins. At the latest follow-up (mean 29 +/- 8 months), 80% of the patients with upper vein isolation remained in sinus rhythm off medications, 62% of the patients maintained sinus rhythm on previously ineffective medications, and 17% continued to be in AF. Fourteen (20%) patients developed intermittent episodes of left atrial flutter, and mapping in these patients revealed large electrically silent areas in the left atrium. Empirical isolation of pulmonary veins appeared to be an effective approach to help maintain sinus rhythm in patients with chronic AF. True electrical isolation of the pulmonary veins was associated with a higher likelihood of long-term success. Left atrial flutter was seen in a significant number of patients at long-term follow-up.

Atrial Fibrillation↗
PubMed2000

First human experience with pulmonary vein isolation using a through-the-balloon circumferential ultrasound ablation system for recurrent atrial fibrillation.

BACKGROUND: Standard mapping and ablation of focal sources of atrial fibrillation are associated with very long procedure times and low efficacy. An anatomic approach to complete pulmonary vein isolation could overcome these limitations. METHODS AND RESULTS: Fifteen patients with atrial fibrillation refractory to medication underwent circumferential isolation of the pulmonary veins by using a novel catheter, with an ultrasound transducer (8-MHz) mounted near the tip, in a saline-filled balloon. Twelve atrial foci and/or atrial fibrillation triggers were identified in 9 patients (pulmonary vein locations: left upper, 3; right upper, 6; right middle, 1; right lower, 1; and left inferior, 1). In 5 patients, lesions were placed in the absence of any mapped triggers. Irrespective of trigger mapping, circumferential isolation of both upper pulmonary veins was attempted in all patients. The lower pulmonary veins were ablated when sinus rhythm activation mapping revealed evidence of a sleeve of atrial muscle in the vein. The median number of lesions per patient required to isolate 1 pulmonary vein was 4 (range, 1 to 29). After ablation, no evidence of narrowing was seen with repeat venography or follow-up computed tomography scan. After a mean follow-up of 35+/-6 weeks, 5 patients had recurrence of atrial fibrillation. Three responded to drugs that were previously ineffective, and 2 remained in atrial fibrillation. CONCLUSIONS: This novel ultrasound ablation system can successfully isolate multiple pulmonary veins. At early follow-up, this approach seems to be effective in preventing recurrent atrial fibrillation in a significant number of patients.

Adult↗
PubMed1998

Interrelations between QRS morphology, duration, and HV interval changes following right bundle branch radiofrequency catheter ablation.

Interrelations between QRS morphology, duration, and HV interval changes in a model of "complete" bundle branch block following right bundle branch radiofrequency ablation have not been subjected to systematic study. This article describes these interrelations in patients who underwent right bundle ablation. Over a period of 42 months, 16 patients underwent radiofrequency ablation of the right bundle for treatment of bundle branch reentrant tachycardia. All 16 patients had prolonged HV interval at baseline (minimum = 60 ms; mean = 68 +/- 8 ms). After ablation, one patient developed complete heart block; the remaining 15 patients developed complete right bundle branch block (RBBB) and further prolongation of the HV interval (increment = 24 +/- 16 ms). In 14 of these 15 patients, QRS duration was 138 +/- 26 ms before ablation and increased to 168 +/- 13 ms after ablation. In the remaining patient, the QRS duration was 160 ms before ablation and shortened to 144 ms following ablation despite further HV prolongation. Larger increases of HV interval after ablation were associated with smaller or negative changes in QRS duration (r = -0.77). Three was a direct relationship between QRS duration at baseline and the increment in HV interval after ablation (r = 0.70), and an inverse relationship between QRS duration before and after ablation (r = 0.84). Radiofrequency ablation of right bundle may be associated with an increase in HV interval and QRS duration. However, HV interval prolongation is not necessarily associated with QRS duration widening. A large change in HV interval is more likely to be associated with an already prolonged QRS duration before ablation and a lesser increase or even decrease in QRS duration after ablation. A shorter QRS duration before ablation is associated with a smaller HV interval increase following ablation but a greater increment in QRS duration. These findings are consistent with the concept that narrowness of QRS duration is due to synchronized activation of ventricular endocardium; whereas, QRS duration widening seen with His-Purkinje damage is due to reduced synchronization of endocardial activation.

Bundle of His↗
PubMed1998

Erosion of implantable cardioverter defibrillator patch electrode into airways: an unusual cause of recurrent hemoptysis.

A 74-year-old man presented with a 9-month history of recurrent hemoptysis. He had implantable cardioverter defibrillator (ICD) patch electrodes placed 4 years before. A chest x-ray film showed crinkling of his posteriorly placed ICD patch which also appeared to have separated from his ventricle on a CT scan of the chest. Bronchoscopy localized the ICD patch electrode to the lower lobe of the left lung. He underwent a lobectomy and was treated with antibiotics at home. In patients with known ICD implantation, patch erosion into the airways should be considered in the differential diagnosis of recurrent hemoptysis.

Aged↗
PubMed1997

Iridium oxide-coated defibrillation electrode: reduced shock polarization and improved defibrillation efficacy.

BACKGROUND: Transvenous implantable cardioverter-defibrillator (ICD) leads are designed to deliver electric shocks to the heart for termination of ventricular dysrhythmias. However, the efficiency of different lead materials has not been well studied. This study compares an ICD lead coated with iridium oxide (IROX), a material that reduces shock-induced polarization, with an otherwise identical, uncoated lead. METHODS AND RESULTS: The defibrillation threshold (DFT) was determined in 13 swine with both IROX-coated and uncoated ICD leads paired with an uncoated "can" electrode. The leads were exchanged through a Teflon sheath to reproduce the intracardiac position. The delivered energy DFT of the IROX-coated lead was 15.9+/-5.4 J and was significantly lower than the delivered energy DFT of the uncoated lead (19.1+/-5.1 J; P<.006). The initial lead impedance was equivalent in both leads (IROX, 41.7+/-5.8 omega; uncoated, 41.3+/-4.7 omega; P=NS) at DFT. However, the impedance rose by 7.3+/-2.0 omega during the first phase and by 3.7+/-2 omega during the second phase with the uncoated lead, whereas the corresponding impedance change was 1.0+/-0.3 omega during phase 1 and 1.6+/-0.5 omega during phase 2 (P<.01 each phase) when the IROX-coated lead was used. CONCLUSIONS: This study shows that an IROX coating of this lead system significantly lowers the DFT energy in the swine model. The blunting of the impedance rise by the IROX coating that is seen is consistent with a reduction in electrode polarization.

Animals↗
PubMed1997

Bundle branch reentry ventricular tachycardia with two distinct left bundle branch block morphologies.

INTRODUCTION: Bundle branch reentry ventricular tachycardia (VT) is usually amenable to treatment with radiofrequency ablation. Different QRS morphologies during VT are possible when anterograde ventricular activation is over the left bundle branch. Manifestations of this reentrant tachycardia with more than one QRS morphology with anterograde activation via the right bundle have not been reported and would be unusual due to the more discrete anatomy of the right bundle branch. METHODS AND RESULTS: An electrophysiologic study was conducted in a patient with dilated ventricle and diminished ventricular function with VT. Typical characteristics of bundle branch reentry were noted when VT was induced. The study was notable for the presence of a right bundle recording only during macroreentrant beats or VT and the distal location of the recording. Radiofrequency ablation was performed. Postablation stimulation again induced VT, proven to be of the same bundle branch reentry mechanism but of a different QRS morphology. A second ablation was required for complete ablation of this patient's bundle branch reentry VT. CONCLUSION: In bundle branch reentry utilizing the left bundle as the retrograde limb and the right bundle branch as the anterograde limb of the circuit, VT of more than one distinct morphology can be seen. Careful evaluation to assess for the persistence of VT of the same mechanism is necessary to ensure complete ablation of the reentrant circuit. Preexisting right bundle disease and a dilated heart with more dispersed distal right bundle branches may predispose to such a phenomenon.

Adult↗
PubMed1995

Atrioventricular nodal conduction gap and dual pathway electrophysiology.

BACKGROUND: The gap phenomenon in atrioventricular (AV) conduction is described as a block that occurs within a range of atrial coupling intervals. This block is assumed to occur between two adjacent parts of the conduction system having different refractory properties; thus, a gap would develop if the functional refractory period of the proximal unit was shorter than the effective refractory period of the distal unit. We describe a new electrophysiological mechanism based on dual pathways electrophysiology of the AV node. METHODS AND RESULTS: In vitro experiments were performed on isolated superfused rabbit hearts. Standard electrophysiological pacing and recording techniques were used to generate conduction curves. The gap phenomenon was documented in 9 of 14 nodal preparations. With shortening of the atrial coupling interval, antegrade conduction block of the "fast" pathway wave front occurred while this impulse was still retrogradely interfering with slow pathway conduction. That is, the fast pathway wave front prevented propagation of the anterograde "slow" pathway wave front by collision or by creating a refractory barrier. This mechanism produced a gap and the block persisted until, at even shorter coupling intervals, the fast wave front penetration became insufficient and conduction was restored through the released slow pathway wave front. This mechanism was verified in AV nodal preparations with separated inputs, in which independent fast and slow wave fronts could be induced and programmed to collide. CONCLUSIONS: Our results established the functional interaction of fast and slow pathway wave fronts as an important electrophysiological mechanism underlying the AV conduction gap. This mechanism may be responsible for a variety of clinically observed conduction discontinuities.

Animals↗
PubMed1995

Long-term clinical outcome of right bundle branch radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia.

The study assessed the long-term outcome of patients undergoing radiofrequency ablation of the right bundle for bundle branch reentrant ventricular tachycardia. Bundle branch reentrant tachycardia was diagnosed in 16 patients (ejection fraction 31% +/- 15%) who underwent electrophysiology study in our laboratory. All patients had His-Purkinje system conduction delay with mean HV interval of 68 +/- 8 ms. After ablation, right bundle branch block developed in 15 patients. One patient developed complete heart block, which was anticipated. One patient died of heart failure 9 months after ablation. Two patients were successfully bridged to heart transplantation 0.5 and 13 months, respectively, after ablation. Two patients received implantable defibrillators for other ventricular tachycardias. One patient had syncope 11 months after ablation, but there was no evidence of ventricular tachycardia or heart block in repeat electrophysiology study. This patient died suddenly 29 months after ablation. The remaining nine patients were alive and well for a mean follow-up of 19 +/- 10 months. Radiofrequency ablation of the right bundle branch is an effective therapy for treatment of bundle branch reentrant ventricular tachycardia. Survival is excellent provided that other types of ventricular tachycardia, when present, are treated as well. This technique may be helpful in management of patients who have unacceptable frequent shocks from their implanted defibrillators and may be helpful in avoiding implantation of such a device completely in others. In some patients with terminal heart failure and incessant ventricular tachycardia, this procedure can function as a bridge to cardiac transplantation.

Adult↗
PubMed1994

Asymmetry of retrograde conduction and reentry within the His-Purkinje system: a comparative analysis of left and right ventricular stimulation.

OBJECTIVES: The purpose of this study was to delineate retrograde His-Purkinje system conduction and reentry (V3 phenomenon) during left ventricular extrastimulation and compare them with right ventricular extrastimulation. BACKGROUND: The V3 phenomenon has been well described in the past during right ventricular extrastimulation; however, it has not been studied systematically during left ventricular extrastimulation. METHODS: Left and right ventricular pacing were performed in 13 patients. Retrograde and anterograde routes of impulse propagation were determined on the basis of the sequence of His (H) and right bundle (RB) potentials, H-RB intervals, as well as the QRS configuration and axis of V3 beats. RESULTS: During right ventricular pacing, retrograde conduction of V2, when discernible, occurred exclusively through the left bundle at all coupling intervals equal to or shorter than the His-Purkinje relative refractory period, with the exception of two isolated beats. During left ventricular extrastimulation, His bundle activation was through the left bundle in nine patients and through the right or left bundle in three other patients. In one patient, the route could not be determined. The V3 phenomena occurred in eight patients during right ventricular pacing. Seven patients had a left bundle branch block pattern QRS configuration, and one had a right bundle branch block pattern configuration. V3 beats occurred in five patients during left ventricular apex pacing: left bundle branch block pattern configuration in one patient and right bundle branch block pattern configuration in four. In three of these four patients, the reentry was interfascicular and limited to the left bundle branch system. CONCLUSIONS: The left-sided His-Purkinje system is the preferred retrograde route of impulse propagation during both left and right ventricular extrastimulation. Reentry within the His-Purkinje system elicited by right ventricular extrastimulation involves both bundle branches, whereas this reentry tends to occur within the left-sided His-Purkinje system during left ventricular pacing.

Adolescent↗
PubMed1993

Implantable cardioverter defibrillator for prevention of sudden cardiac death in patients with ventricular tachycardia and ventricular fibrillation: ICD therapy in sudden cardiac death.

Among the various therapy options for survivors of ventricular tachycardia-ventricular fibrillation (VT-VF), the implantable cardioverter defibrillator (ICD) seems most promising. It reliably terminates VT-VF and thus significantly impacts sudden cardiac death (SCD) survival. It is more effective than any of the known antiarrhythmic drugs in prevention of SCD, particularly among survivors of cardiac arrest. Compared to VT surgery, the ICD therapy can be offered to a larger pool of patients and can be placed at a lower surgical risk. With proper patient selection, ICD therapy is of major benefits to its recipients since it markedly reduces the chances of VT-VF related mortality; the main cause of premature death in this population. The ICD therapy is cost effective when compared to other medical interventions and could be more so if the implant is carried out early in the course of VT-VF management.

Death, Sudden, Cardiac↗
PubMed1992

Induction of ventricular fibrillation versus monomorphic ventricular tachycardia during programmed stimulation. Role of premature beat conduction delay.

BACKGROUND: Premature stimuli can cause ventricular fibrillation (VF) during electrophysiological testing. The electrophysiological correlations associated with the onset of VF were evaluated in 40 patients who had this rhythm induced during programmed ventricular stimulation. These parameters were compared with those observed in 51 patients who had inducible sustained monomorphic ventricular tachycardia (VT) and 45 patients who had no inducible sustained ventricular tachyarrhythmias. METHODS AND RESULTS: Shortest premature coupling intervals for S2, S3, and S4 at induction of tachycardia or before achieving refractoriness, corresponding conduction latencies (defined as the time from the premature stimulus to the upstroke of the depolarization wave front recorded 35 mm away from the stimulation site), and ventricular activation times (defined as the time from the premature stimulus to the end of the depolarization wave) were compared. The mean coupling intervals were longest in the inducible VT patients: 300 +/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively. In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/- 20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194 +/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The coupling interval of the last premature extrastimulus was above 200 msec in 70% of the patients in whom VF was induced. The largest increases in latency and activation times were recorded in patients in whom VF was induced. The cumulative increase in latency, defined as increased conduction time from baseline, summed for all the premature stimuli was also the greatest at initiation of VF. In contrast, the smallest increases in these parameters were noted in the patients with no inducible VT or VF. Measurements of total activation time yielded similar results as those recorded for latencies. The most important parameters distinguishing the VT patient population from the other two groups were the low ejection fractions and the longer coupling intervals at which VT was induced, whereas in the VF group, the most important discriminating factor was cumulative activation time. Sixty-three percent of the inducible VF patients presented with abnormal hearts (myocardial infarction or cardiomyopathy), whereas 88% of the inducible VT patients had abnormal hearts. In contrast, only 25% of the patients in whom no arrhythmia was induced presented with abnormal hearts. Mean ejection fraction was 32 +/- 15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and 51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus VT). CONCLUSIONS: The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.

Cardiac Complexes, Premature↗
PubMed1992

Iontophoretic transmyocardial drug delivery. A novel approach to antiarrhythmic drug therapy.

BACKGROUND: Antiarrhythmic drugs often fail to achieve therapeutic effects without toxic systemic levels. Direct transport of drugs into the myocardium may circumvent this problem and may also provide new insights into antiarrhythmic drug effect on arrhythmogenic tissues. In a canine model, procainamide (PA) was delivered iontophoretically using pulsed current synchronized with the ventricular depolarization via an implantable defibrillator patch electrode that was modified to contain a 3.6-ml chamber. Myocardial tissue concentrations of PA were evaluated in 7-day myocardial infarcts (n = 16) that were exposed to 10 minutes of iontophoretic PA delivery and compared with passive diffusion (n = 5) and intravenous (n = 16) PA. These dogs were followed for 3 hours. The infarcted tissue PA levels were compared with normal myocardium. Coronary and systemic blood levels of PA, effective refractory period (ERP), diastolic threshold, and efficacy of ventricular tachycardia (VT) suppression were evaluated throughout the follow-up period. METHODS AND RESULTS: Three hours after 10 minutes of iontophoretic, passive, and intravenous PA, the epicardial layer concentration in the center of the infarcted zone was 840 +/- 853 micrograms/g, 93 +/- 90 micrograms/g, and 15 +/- 8 micrograms/g of tissue, respectively. In the endocardial layer, the PA concentrations with iontophoresis were 38 +/- 57 micrograms/g and were significantly higher than those achieved with either passive diffusion 38 +/- (4 +/- 2 micrograms/g) or with intravenous delivery (11 +/- 5 micrograms/g) (p less than 0.05). Epicardial tissue PA concentrations 3 hours after iontophoresis, passive diffusion, and intravenous PA in the normally perfused tissues were 14 +/- 13 micrograms/g, 3 +/- 2 micrograms/g, and 16 +/- 8 micrograms/g of PA, respectively. Venous blood levels were 2 +/- 3 micrograms/ml 3 hours after iontophoresis, 1 +/- 1 microgram/ml 3 hours after passive PA delivery, and 11 +/- 7 micrograms/ml with intravenous administration (p less than 0.05 intravenous versus passive and iontophoresis). Iontophoretic delivery of PA resulted in 22 +/- 29 msec ERP prolongation intramurally in the infarcted zone with no significant normal tissue ERP prolongation. Passive delivery of PA produced no significant changes in ERP. After intravenous infusion, the ERP in the infarcted zone increased by 35 +/- 29 msec and 13 +/- 12 msec in the normal tissue. Sustained monomorphic VT was induced in 20 animals. In one of these animals, only nonsustained VT could be induced at baseline; however, after intravenous PA, VT could be induced and remained inducible throughout the 3-hour follow-up period. In the iontophoretic delivery group, PA suppressed VT in all of the animals, with termination time ranging from 20 seconds to 7 minutes. In three cases, sustained monomorphic VT could be reinduced, two after 60 minutes and one after 120 minutes. However, in seven dogs, VT could not be induced during the 3-hour follow-up period. None of the dogs in which PA was delivered iontophoretically into the infarcted myocardium developed VT that was not induced before delivery of the drug. Intravenous PA administration resulted in VT suppression in one of 10 dogs. In two dogs, VT could not be induced before intravenous infusion of PA. However, after intravenous PA, VT could be induced. Immunohistochemical mapping of the PA within the infarcted tissue revealed transmural PA distribution. CONCLUSIONS: These data show that 1) the delivery of high transmural concentrations of PA directly into infarcted myocardium is both feasible and effective...

Animals↗
PubMed1992

Localization of the fast and slow pathways in atrioventricular nodal reentrant tachycardia by intraoperative ice mapping.

BACKGROUND: Atrioventricular (AV) nodal reentrant tachycardia is classically described as a reentrant rhythm entirely contained within the compact AV node. Although the concepts of longitudinal dissociation of two intranodal pathways and a distal common pathway are accepted, the proximal portion of the circuit remains undefined. Current reports suggest that the two pathways may be separable by atrial tissue and not contained entirely within the compact node. METHODS AND RESULTS: We used an ice mapping method to demonstrate the slow and fast pathways of the reentrant circuit and their relation to the atrial septum around the AV node. Six patients with the usual form (slow-fast) of AV nodal reentrant tachycardia were mapped during surgery. In most patients, antegrade slow pathway localization was posterior and inferior to the compact AV node along the tricuspid annulus; in two patients, it was superior along the tendon of Todaro. Retrograde fast pathway localization was anterior or superior to the compact AV node in all patients. In all patients, anatomic distinction was made between the two pathways and the compact node. CONCLUSIONS: We conclude that no upper common pathway exists within the compact AV node in the usual type of nodal reentrant tachycardia and that the perinodal atrial tissue is a requisite part of the tachycardia circuit.

Adolescent↗
PubMed1992

Role of implantable cardioverter defibrillator therapy in the management of high-risk patients.

Cardiovascular mortality from ventricular tachycardia (VT) and ventricular fibrillation (VF) continues to be a major health problem. Several therapeutic approaches are now available to treat patients with known VT/VF. Among the various therapeutic options are antiarrhythmic drugs, catheter or surgical ablation of VT focus, and implantable cardioverter defibrillator (ICD). The overall 2-year cardiovascular mortality is significantly reduced by ICD therapy. The ICD is particularly useful in patients with 1) no inducible but clinical VT/VF, 2) drug refractory VT/VF, and 3) VT/VF in association with left ventricular ejection fraction of less than or equal to 30%. Significant improvements in ICD therapy have already been made; these improvements include tiered antitachycardia therapy, antibradycardia pacing, lower defibrillation threshold, and longer life of generator. Further improvements are expected, including nonthoracotomy approach to defibrillation, pectoral implant, and dual chamber sensing. It is likely that with all of the advances in ICD therapy its acceptance as a therapeutic option will increase.

Costs and Cost Analysis↗
PubMed1991

When is it safe not to replace an implantable cardioverter defibrillator generator?

In most reports on patients receiving implantable cardioverter defibrillators, shocks were received mainly during the first 2 to 3 years. Thus, the question had been raised as to the need for device replacement after 3 or 4 years if no shocks had been received. In order to answer this question, shock experience in 184 patients receiving the implantable cardioverter defibrillator was analyzed. Patients were followed for a mean of 24 +/- 18.7 months. A patient's shock was judged to be appropriate if there was electrocardiographic documentation of sustained ventricular tachyarrhythmia at the time of shock or if it was preceded by sudden onset of presyncopal or syncopal symptoms. The majority of patients had coronary artery disease. In approximately two-thirds of patients, left ventricular ejection fraction was below 40%. One hundred fourteen patients had inducible sustained monomorphic ventricular tachycardia. On follow-up, there were 29 deaths, five of which were sudden. Sixty-eight patients received an appropriate shock during follow-up (37%). Over 90% of these 68 received their first shock within the 2 years after implant. The actuarial risk of receiving an appropriate shock by the fifth year after implant was 69%. Conversely, 31% of patients who survived 5 years had not received an appropriate shock. Hazard analysis indicates that there is a high incidence of first appropriate shock during the year following implant. Subsequently, the incidence dropped to a relatively steady rate with a rise in this rate during the fifth year. This analysis suggested a bimodal distribution of appropriate shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1991

Does reception of appropriate shocks from the implantable cardioverter defibrillator affect survival?

The implantable cardioverter defibrillator has become an important therapeutic modality for treatment of life-threatening ventricular tachyarrhythmias. Recent reports have suggested that patients who receive appropriate shocks from this device have an inordinately high overall mortality, and questioned the extent of benefit these patients derive from the implant. This report analyzed the survival among 184 patients who received the implantable cardioverter defibrillator to assess survival differences between patients who received appropriate shocks versus those who did not. At a mean follow-up of 24 +/- 18.7 months, 68 patients received an appropriate shock from their device while 116 did not receive an appropriate shock. Overall survival of the entire population was quite similar to those published by others. There was no significant difference between overall survival of patients who received an appropriate shock versus those who did not. However, there was a statistically significant difference in sudden death mortality. The group of patients that received appropriate shocks included all five sudden deaths. This observation suggested that sudden death in this population was likely due to ventricular tachyarrhythmias rather than strictly bradycardia or asystole. The "benefit" of the device to the entire population was also assessed by estimating survival after receipt of the first appropriate shock. Using this approach, an estimated 10% of patients died without receiving an appropriate shock. In other words, ultimately, 90% of patients were expected to benefit from the device. This survival curve, which initiated only after receipt of the first appropriate shock was fairly similar to those estimated from conventional methods. Therefore, survival after receipt of an appropriate shock was comparable to overall survival and there was no significant difference between survival of patients who received appropriate shocks and those who did not.

Death, Sudden, Cardiac↗